Matches in SemOpenAlex for { <https://semopenalex.org/work/W4282842698> ?p ?o ?g. }
- W4282842698 abstract "Abstract Background Innate immunity genes have been reported to affect susceptibility to inflammatory bowel diseases (IBDs) and colitis in mice. Dectin-1, a receptor for fungal cell wall β-glucans, has been clearly implicated in gut microbiota modulation and modification of the susceptibility to gut inflammation. Here, we explored the role of Dectin-1 and Dectin-2 (another receptor for fungal cell wall molecules) deficiency in intestinal inflammation. Design Susceptibility to dextran sodium sulfate (DSS)-induced colitis was assessed in wild-type, Dectin-1 knockout (KO), Dectin-2KO, and double Dectin-1KO and Dectin-2KO (D-1/2KO) mice. Inflammation severity, as well as bacterial and fungal microbiota compositions, was monitored. Results While deletion of Dectin-1 or Dectin-2 did not have a strong effect on DSS-induced colitis, double deletion of Dectin-1 and Dectin-2 significantly protected the mice from colitis. The protection was largely mediated by the gut microbiota, as demonstrated by fecal transfer experiments. Treatment of D-1/2KO mice with opportunistic fungal pathogens or antifungal agents did not affect the protection against gut inflammation, suggesting that the fungal microbiota had no role in the protective phenotype. Amplicon-based microbiota analysis of the fecal bacterial and fungal microbiota of D-1/2KO mice confirmed the absence of changes in the mycobiota but strong modification of the bacterial microbiota. We showed that bacteria from the Lachnospiraceae family were at least partly involved in this protection and that treatment with Blautia hansenii was enough to recapitulate the protection. Conclusions Deletion of both the Dectin-1 and Dectin-2 receptors triggered a global shift in the microbial gut environment, affecting, surprisingly, mainly the bacterial population and driving protective effects in colitis. Members of the Lachnospiraceae family seem to play a central role in this protection. These findings provide new insights into the role of the Dectin receptors, which have been described to date as affecting only the fungal population, in intestinal physiopathology and in IBD." @default.
- W4282842698 created "2022-06-15" @default.
- W4282842698 creator A5013288442 @default.
- W4282842698 creator A5018850767 @default.
- W4282842698 creator A5023888124 @default.
- W4282842698 creator A5027955775 @default.
- W4282842698 creator A5034583740 @default.
- W4282842698 creator A5047571737 @default.
- W4282842698 creator A5060553658 @default.
- W4282842698 creator A5065755459 @default.
- W4282842698 creator A5073396022 @default.
- W4282842698 creator A5075601406 @default.
- W4282842698 creator A5076433007 @default.
- W4282842698 creator A5083701333 @default.
- W4282842698 date "2022-06-14" @default.
- W4282842698 modified "2023-10-18" @default.
- W4282842698 title "Deletion of both Dectin-1 and Dectin-2 affects the bacterial but not fungal gut microbiota and susceptibility to colitis in mice" @default.
- W4282842698 cites W1520655088 @default.
- W4282842698 cites W1541292363 @default.
- W4282842698 cites W1579566330 @default.
- W4282842698 cites W1988820663 @default.
- W4282842698 cites W1995053980 @default.
- W4282842698 cites W2036743290 @default.
- W4282842698 cites W2050445005 @default.
- W4282842698 cites W2056450591 @default.
- W4282842698 cites W2067954786 @default.
- W4282842698 cites W2072970694 @default.
- W4282842698 cites W2076794463 @default.
- W4282842698 cites W2089422083 @default.
- W4282842698 cites W2113576692 @default.
- W4282842698 cites W2124351063 @default.
- W4282842698 cites W2133856765 @default.
- W4282842698 cites W2136420871 @default.
- W4282842698 cites W2160947363 @default.
- W4282842698 cites W2164514035 @default.
- W4282842698 cites W2179438025 @default.
- W4282842698 cites W2191014442 @default.
- W4282842698 cites W2260815707 @default.
- W4282842698 cites W2346752870 @default.
- W4282842698 cites W2732940013 @default.
- W4282842698 cites W2774551105 @default.
- W4282842698 cites W2804166434 @default.
- W4282842698 cites W2889353502 @default.
- W4282842698 cites W2900030356 @default.
- W4282842698 cites W2918402014 @default.
- W4282842698 cites W2919677651 @default.
- W4282842698 cites W2964800211 @default.
- W4282842698 cites W3016889019 @default.
- W4282842698 cites W3049537585 @default.
- W4282842698 cites W3127288224 @default.
- W4282842698 cites W4366807451 @default.
- W4282842698 doi "https://doi.org/10.1186/s40168-022-01273-4" @default.
- W4282842698 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35698210" @default.
- W4282842698 hasPublicationYear "2022" @default.
- W4282842698 type Work @default.
- W4282842698 citedByCount "6" @default.
- W4282842698 countsByYear W42828426982022 @default.
- W4282842698 countsByYear W42828426982023 @default.
- W4282842698 crossrefType "journal-article" @default.
- W4282842698 hasAuthorship W4282842698A5013288442 @default.
- W4282842698 hasAuthorship W4282842698A5018850767 @default.
- W4282842698 hasAuthorship W4282842698A5023888124 @default.
- W4282842698 hasAuthorship W4282842698A5027955775 @default.
- W4282842698 hasAuthorship W4282842698A5034583740 @default.
- W4282842698 hasAuthorship W4282842698A5047571737 @default.
- W4282842698 hasAuthorship W4282842698A5060553658 @default.
- W4282842698 hasAuthorship W4282842698A5065755459 @default.
- W4282842698 hasAuthorship W4282842698A5073396022 @default.
- W4282842698 hasAuthorship W4282842698A5075601406 @default.
- W4282842698 hasAuthorship W4282842698A5076433007 @default.
- W4282842698 hasAuthorship W4282842698A5083701333 @default.
- W4282842698 hasBestOaLocation W42828426981 @default.
- W4282842698 hasConcept C111289621 @default.
- W4282842698 hasConcept C142724271 @default.
- W4282842698 hasConcept C203014093 @default.
- W4282842698 hasConcept C2775862500 @default.
- W4282842698 hasConcept C2776914184 @default.
- W4282842698 hasConcept C2777695942 @default.
- W4282842698 hasConcept C2778260677 @default.
- W4282842698 hasConcept C2779134260 @default.
- W4282842698 hasConcept C2779341262 @default.
- W4282842698 hasConcept C2779704485 @default.
- W4282842698 hasConcept C42062724 @default.
- W4282842698 hasConcept C523546767 @default.
- W4282842698 hasConcept C539455810 @default.
- W4282842698 hasConcept C54355233 @default.
- W4282842698 hasConcept C71924100 @default.
- W4282842698 hasConcept C86803240 @default.
- W4282842698 hasConcept C8891405 @default.
- W4282842698 hasConcept C89423630 @default.
- W4282842698 hasConceptScore W4282842698C111289621 @default.
- W4282842698 hasConceptScore W4282842698C142724271 @default.
- W4282842698 hasConceptScore W4282842698C203014093 @default.
- W4282842698 hasConceptScore W4282842698C2775862500 @default.
- W4282842698 hasConceptScore W4282842698C2776914184 @default.
- W4282842698 hasConceptScore W4282842698C2777695942 @default.
- W4282842698 hasConceptScore W4282842698C2778260677 @default.
- W4282842698 hasConceptScore W4282842698C2779134260 @default.
- W4282842698 hasConceptScore W4282842698C2779341262 @default.
- W4282842698 hasConceptScore W4282842698C2779704485 @default.